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The incremental gain from dual/triple agonists appears to be 58 percentage points of body weight ( [18] )

For example, endothelium-derived NO directly suppresses the electrical excitability of VSMCs by inhibiting the action of T-type and L-type voltage-gated Ca 2+ channels in small arteries, and reduced NO availability can trigger transient depolarization in normally quiescent VSMCs leading to vasospasm (Smith et al., 2020)